DESCRIPTION (Applicant's abstract): Our long-term objective is understanding exercise training-induced vascular adaptation in skeletal muscle. Ongoing research provides new insight to relationships among regional vascular adaptations to exercise, muscle fiber types, oxidative capacity, vascularization, muscle fiber recruitment patterns during exercise and the resulting specificity of adaptations induced by different exercise training programs. Data indicate that vascular adaptations are most evident in skeletal muscle tissue with the greatest relative increase in activity during training bouts. Exercise training induces an increase in vascular transport capacity: both blood flow (BF) and capillary exchange capacity are increased. Aim 1 experiments will determine whether mechanisms for training-induced increases in BF capacity include: a) enhanced endothelium-mediated dilation due to increased expression of endothelial nitric oxide synthase (ecNOS), b) altered vasoconstrictor responsiveness, c) increased arteriolar density, and d) whether increases circumferential wall stress during exercise is the signal for structural adaptation. Vasomotor responsiveness and endothelium-mediated control mechanisms will be examined in vitro in isolated arterioles of different branch orders (1A, 2A, 3A, etc). Research proposed for Aim 2 will use RT-PCR to assess ecNOS gene expression in single arterioles to test the following hypotheses: a) ecNOS-mRNA expression increases with branch order in the arteriolar network, b) endurance training increases ecNOS-mRNA expression in arterioles of high-oxidative muscle, c) sprint training increases ecNOS-mRNA expression in arterioles of white (FG) muscle, and d) increased flow through single isolated arterioles can stimulate increased expression of ecNOS-mRNA. Aim 3 will determine whether exchange vessel permeability of red muscle is greater than in white muscle and test the hypothesis that exercise training increases microvascular permeability and alters control of permeability via endothelium-dependent regulation of permeation in skeletal muscle. Application of molecular techniques and concepts will establish mechanisms for differences in phenotype along the arterial tree and for training-induced changes in phenotype of endothelium and VSM in skeletal muscle arterioles.